Approximately 5,000,000 North Americans harbor intracranial aneurysms. The estimated annual rate of aneurysm rupture is about 10-28 per 100,000. Unfortunately, aneurysm ruptures are currently associated with relatively high morbidity and mortality. A large, international study reporting the results from surgical and medical management of patients admitted to neurosurgical services during a multi-year period in the early 1980s, revealed a mortality and morbidity rate of 42% among the North American patients. N. F. Kassell and J. C. Torner, The International Cooperative Study on the Timing of Aneurysm Surgery—an Update, 23 STROKE 205, 210 (1992). Therapeutic approaches to the treatment of subarachnoid hemorrhage have improved only modestly in the 40 years since this study. Among the many severe complications of subarachnoid hemorrhage, arterial narrowing resulting from cerebral vasospasm is perhaps the most pervasive and deleterious. This complication develops in about 40-70% of patients with aneurysmal subarachnoid hemorrhage and causes a delayed ischemic deficit in about 20-30% of those patients. It is generally considered to be the leading cause of mortality and morbidity in patients who have survived their initial hemorrhage.
A variety of treatments have been clinically tested for preventing cerebral vasospasm, reducing the severity of cerebral vasospasm, and/or reducing the ischemic effects of cerebral vasospasm. Tested therapeutic agents intended to prevent cerebral vasospasm or to reduce the severity of cerebral vasospasm include certain calcium channel blockers, endothelin receptor antagonists, and antispasmodics. These agents have mostly either failed to cause improved outcomes or provided only short lived effects. Nimodipine (a calcium channel blocker) and papaverine (an antispasmodic) have shown some promise, but still have little or no potential for robust prevention of cerebral vasospasm. Tested therapeutic agents intended to reduce the ischemic effects of cerebral vasospasm include certain N-methyl D-aspartate receptor antagonists and free radical scavengers. To date, these agents have also failed to significantly improve outcomes.
Since no single agent has been shown to be highly effective for improving outcomes following subarachnoid hemorrhage, standard treatments currently include a combination of therapies. The Triple-H therapy, which involves intravascularly administering a combination of drugs and fluid to induce hypervolemia, hypertension, and hemodilution, is currently the most widely used treatment. This approach is intended to increase blood flow through vasospastic vessels and thereby increase blood delivery to ischemic areas of the brain. Transluminal balloon angioplasty of major intracerebral arteries is also used in some cases with the same objective. Although useful, the Triple-H therapy and transluminal balloon angioplasty at best only partially reduce the ischemia associated with cerebral vasospasm. Their effect is often insufficient to prevent neurological impairment or even death. Furthermore, these approaches can have significant complications. For example, the Triple-H therapy can increase the rate of pulmonary edema, myocardial ischemia, hyponatremia, renal medullary washout, cerebral edema, and additional cerebral hemorrhage. Transluminal balloon angioplasty can increase the risk of surgically induced neurological damage, infection, and vessel stenosis.
Addressing cerebral vasospasm directly (e.g., preventing cerebral vasospasm or reducing the severity of cerebral vasospasm) has much greater potential for improving outcomes than merely mitigating the corresponding ischemic effects. Furthermore, since cerebral vasospasm typically has a delayed onset and a relatively gradual clinical course after hemorrhage (e.g., following aneurysm rupture), in most cases, there is a window of opportunity to apply preventative therapies. An effective approach for preventing cerebral vasospasm or reducing the severity of cerebral vasospasm has the potential annually to save thousands of lives and to prevent thousands of cases of neurological impairment. Accordingly, for this reason and/or for other reasons not stated herein, there is a need for innovation with respect to devices, systems, and methods for treating subarachnoid hematoma, cerebral vasospasm, and/or other related conditions.